Multiple thrombogenic and atherogenic markers were involved in premature coronary artery disease

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorMANSUR, A. P.
dc.contributor.authorTAKADA, J. Y.
dc.contributor.authorSTRUNZ, C. M. C.
dc.contributor.authorAVAKIAN, S. D.
dc.contributor.authorCESAR, L. A. M.
dc.contributor.authorRAMIRES, J. A. F.
dc.date.accessioned2013-10-11T21:17:40Z
dc.date.available2013-10-11T21:17:40Z
dc.date.issued2012
dc.description.abstractAtherogenic and thrombogenic factors are implicated in the pathogenesis of coronary artery disease (CAD). Polymorphisms in the lymphotoxin-alfa (LTA) gene, a pro-inflammatory cytokine, have been also associated with susceptibility to myocardial infarction, but results in different studies are conflicting. We examined the association of atherothrombotic markers and the LTA promoter A252G polymorphism with risk of premature CAD. Methods: A case-control study was conducted in 336 patients with documented premature CAD and 189 unrelated health controls both with less than 50 years old. Clinical characteristics and laboratorial data which included thrombogenic factors (fibrinogen, protein C, protein S and antithrombin III); and atherogenic factors (fasting glucose, lipid profile; lipoprotein (a), apolipoproteins AI and B fractions) were evaluated. Genetic variability of LTA was determined by polymerase chain reaction. Results: Male, history of premature CAD, smoking status, diabetes, hypertension and dyslipidemia were significantly more prevalent in the CAD group. Compared with controls, CAD cases had significantly lower mean concentrations of apolipoprotein AI (1.34±0.21 vs 1.23±0.22 mg/dL;<0.01), HDL-cholesterol (46.4±11.9 vs 41.1±11.2 mg/dL; p<0.01) and antithrombin III(100±12.7 vs 94.2±17.8%; p=0.02), and higher plasma concentration of fasting glucose (103.3±26.9 vs 112.1±45.3 mg/dL; p<0.01) and Lipoprotein (a) levels(32.8±32.6 vs 50.1±49.2 mg/dL; p<0.01). The LTA A252G polymorphism frequency for AA, AG and GG was respectively 55.0%, 37,6%, and 7.4% for control group and 42.7%, 46.0% and 11.3% for patients group (p=0.02). A multivariable logistic regression analysis showed that hypertension (OR 2.19 95% CI 1.290-3.716), smoker (OR 2.18; 95% CI 1.455-3.277), dyslipidemia (OR 1.94; 95% CI1.233-3.072), family history (OR 7.13; 95% CI 4.383-11.606) and LTA polymorphism (OR 1.88; 95% CI 1.193-2.972) were independent risk factors for susceptibility to CAD. LTA mutant was risk marker for CAD only in male without the traditional risk factors. Conclusions: Worse traditional risk factors profile and atherothrombogenic markers were associated with susceptibility to premature CAD. LTA mutant allelic was independently associated with premature CAD in male in the absence of traditional risk factors. Premature CAD was associated with worse clinical and laboratory multimarkers.
dc.description.conferencedateAUG 25-29, 2012
dc.description.conferencelocalMunchen, GERMANY
dc.description.conferencenameCongress of the European-Society-of-Cardiology (ESC)
dc.description.indexMEDLINE
dc.identifier.citationEUROPEAN HEART JOURNAL, v.33, suppl.1, p.304-305, 2012
dc.identifier.issn0195-668X
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/2773
dc.language.isoeng
dc.publisherOXFORD UNIV PRESS
dc.relation.ispartofEuropean Heart Journal
dc.rightsrestrictedAccess
dc.rights.holderCopyright OXFORD UNIV PRESS
dc.subject.wosCardiac & Cardiovascular Systems
dc.titleMultiple thrombogenic and atherogenic markers were involved in premature coronary artery disease
dc.typeconferenceObject
dc.type.categorymeeting abstract
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.contributor.author-fmusphcANTONIO DE PADUA MANSUR
hcfmusp.contributor.author-fmusphcJULIO YOSHIO TAKADA
hcfmusp.contributor.author-fmusphcCELIA MARIA CASSARO STRUNZ
hcfmusp.contributor.author-fmusphcSOLANGE DESIREE AVAKIAN MANSUR
hcfmusp.contributor.author-fmusphcLUIZ ANTONIO MACHADO CESAR
hcfmusp.contributor.author-fmusphcJOSE ANTONIO FRANCHINI RAMIRES
hcfmusp.description.beginpage304
hcfmusp.description.endpage305
hcfmusp.description.issuesuppl 1
hcfmusp.description.volume33
hcfmusp.origemWOS
hcfmusp.origem.wosWOS:000308012402460
hcfmusp.publisher.cityOXFORD
hcfmusp.publisher.countryENGLAND
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relation.isAuthorOfPublication.latestForDiscovery534e7a71-d47f-470a-aff1-b3666c694da4
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